Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

摘要: Chemokine CCL24, acting through receptor CCR3, is a potent chemoattractant for eosinophil in allergic diseases and parasitic infections. We recently reported that CCL24 CCR3 are co-expressed by trophoblasts human early pregnant uterus. Here we prove with evidence steroid hormones estradiol (E), progesterone (P), chorionic gonadotropin (hCG), as well decidual stromal cells (DSCs) could regulate the expression of trophoblasts. further investigate how trophoblast-derived mediates function vitro, conclude CCL24/CCR3 promotes proliferation, viability invasiveness In addition, analysis downstream signaling pathways show extracellular signal-regulated kinases (ERK1/2) phosphoinositide 3-kinase (PI3K) may contribute to activating intracellular molecules Ki67 matrix metallopeptidase 9 (MMP9). However, did not observe any inhibitory effect on when blocking c-Jun N-terminal kinase (JNK) or p38 pathways. conclusion, our data suggests at maternal-fetal interface cell growth ERK1/2 PI3K Meanwhile, pregnancy-related (P hCG), DSCs up-regulate trophoblasts, which indirectly influence biological functions Thus, results provide possible explanation invasion embryo implantation.